Evidence map›Paper›PMID 8991089›Full record

ArticleThe Journal of cell biology1996

Multiple PEX genes are required for proper subcellular distribution and stability of Pex5p, the PTS1 receptor: evidence that PTS1 protein import is mediated by a cycling receptor.

G Dodt, S J Gould

Abstract read
In one paragraph

Article in The Journal of cell biology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers.

0numbers the graph read from it
0cells of the map it votes in
101citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

101 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. PEX1 is essential for glycosome biogenesis and trypanosomatid parasite survival.Frontiers in cellular and infection microbiology · 2024
    Article
  6. Article
  7. Article
  8. Article
  9. Association of genetic variants ofAnnals of translational medicine · 2021
    Article
  10. Membrane Interactions of the Peroxisomal Proteins PEX5 and PEX14.Frontiers in cell and developmental biology · 2021
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. AProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  19. Review
  20. Article

41 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

G DodtDepartment of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
S J Gould

Funding

MOLECULAR ANALYSIS OF PEROXISOME ASSEMBLYR01DK045787 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI GOULD, STEPHEN J · 1993 to 2011
$4.7M
NIDDK NIH HHS DK45787
6 · The paper itself

Abstract

PEX5 encodes the type-1 peroxisomal targeting signal (PTS1) receptor, one of at least 15 peroxins required for peroxisome biogenesis. Pex5p has a bimodal distribution within the cell, mostly cytosolic with a small amount bound to peroxisomes. This distribution indicates that Pex5p may function as a cycling receptor, a mode of action likely to require interaction with additional peroxins. Loss of peroxins required for protein translocation into the peroxisome (PEX2 or PEX12) resulted in accumulation of Pex5p at docking sites on the peroxisome surface. Pex5p also accumulated on peroxisomes in normal cells under conditions which inhibit protein translocation into peroxisomes (low temperature or ATP depletion), returned to the cytoplasm when translocation was restored, and reaccumulated on peroxisomes when translocation was again inhibited. Translocation inhibiting conditions did not result in Pex5p redistribution in cells that lack detectable peroxisomes. Thus, it appears that Pex5p can cycle repeatedly between the cytoplasm and peroxisome. Altered activity of the peroxin defective in CG7 cells leads to accumulation of Pex5p within the peroxisome, indicating that Pex5p may actually enter the peroxisome lumen at one point in its cycle. In addition, we found that the PTS1 receptor was extremely unstable in the peroxin-deficient CG1, CG4, and CG8 cells. Altered distribution or stability of the PTS1 receptor in all cells with a defect in PTS1 protein import implies that the genes mutated in these cell lines encode proteins with a direct role in peroxisomal protein import.

Indexed as

Biological TransportCell CompartmentationCell LineCytoplasmFibroblastsFluorescent Antibody TechniqueHumansMicrobodiesPeroxisome-Targeting Signal 1 ReceptorReceptors, Cytoplasmic and NuclearSkinSubcellular FractionsPeroxisome-Targeting Signal 1 ReceptorPEX5 protein, humanReceptors, Cytoplasmic and Nuclear

Identifiers

PMID8991089
PMCPMC2133940

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.